Clinical specimens showed that CRC with KRAS mutations exhibited a higher density of Tregs compared to wild‐type tumors.[50] In vivo experiments demonstrated that KRAS G12C, G12D, and G12V promoted the secretion of IL‐10 and TGF‐β1 through the MEK‐ERK signaling pathway, facilitating the conversion of CD4+ T cells into Treg phenotypes.[50, 51] Macrophages, key components of the tumor immune microenvironment, can switch between pro‐tumor and antitumor states. The gene discussed is TGFB1; the disease is neoplasm.